Direct recruitment of PI3K to p-KIT

The regulatory subunit (p85) of PI3K interacts directly with phosphorylated Y721 of KIT via one of its SH2 domains. This binding leads to the activation of the catalytic domain (p110) of PI3K. SCF-induced PI3K recruitment mediates AKT activation through phospholipids at the membrane and to subsequent phosphorylation of the pro-apoptotic factor Bad as well as Fox3a.<br>PI3K activation mediates SCF-induced cell proliferation, survival, differentiation, adhesion, secretion and actin cytoskeletal organization.

PI3K（磷脂酰肌醇3激酶）的调控亚基（p85）通过与KIT蛋白的磷酸化Y721位点直接相互作用，其SH2结构域之一介导此结合。该结合进而导致PI3K催化域（p110）的激活。SCF（干细胞因子）诱导的PI3K募集通过质膜上的磷脂介导AKT的激活，以及随后促凋亡因子Bad和Fox3a的磷酸化。PI3K的激活通过SCF诱导细胞增殖、存活、分化、粘附、分泌以及细胞骨架的肌动蛋白组织。